George Truskey is the R. Eugene and Susie E. Goodson Professor and Senior Associate Dean for Research in the Pratt School of Engineering. Dr. Truskey's research interests include cardiovascular tissue engineering, microphysiological systems, and the mechanisms of atherogenesis. He also studies cell adhesion and cell biomechanics, for which he focuses upon the effect of flow on endothelial cell adhesion to synthetic surfaces and monocyte adhesion to endothelium. He received a PhD degree in 1985 from MIT. He has been a faculty member in the Department of Biomedical Engineering at Duke since 1987. From 2003-2011, he was Chair of the Department of Biomedical Engineering at Duke University. He is the author of over 110 peer-reviewed research publications, a biomedical engineering textbook entitled Transport Phenomena in Biological Systems, six book chapters, over 180 research abstracts and presentations, 1 patent and 2 patent applications. He is a Fellow of the Biomedical Engineering Society (BMES), the American Institute of Medical and Biological Engineering, and the American Heart Association. He was president of BMES from 2008 to 2010. He received the Capers and Marion McDonald Award for Excellence in Mentoring and Advising from the Pratt School of Engineering at Duke (2007) and the BMES Distinguished Service Award (2012).

Human Microphysiological Systems for Disease Modeling

Human microphysiological systems that use cells from individuals with a range of disease can address limitations of existing animal models that incompletely replicate the disease phenotype. We have cultured primary and induced pluripotent stem (iPS) cells to model features of a genetic disease, Hutchison-Gilford Progeria Syndrome (HGPS), a rare, accelerated aging disorder caused by an altered form of the lamin A (LMNA) gene termed progerin, exhibited expression of progerin. Smooth muscle cells and endothelial cells differentiated from iPS cells maintained key features of the mature phenotype for a number of passages. Cells derived from patients with HGPS showed reduced growth rate and increased cell death. Since the major cause of death in HGPS arises from accelerated atherosclerosis, we developed an arteriole-scale endothelialized tissue engineered blood vessel (TEBV) with inner diameter of 800 µm. eTEBVs fabricated with smooth muscle cells from individuals with HGPS show reduced vasoactivity, increased medial wall thickness, increased calcification and apoptosis in comparison to eTEBVs fabricated with smooth muscle cells from normal individuals or primary MSCs. Both the endothelium and smooth muscle cells contributed to disease pathology. Treatment with a number of compounds being considered for clinical trials reversed the disease progression and improved the cellular content and function of the eTEBVs. These results indicate that iPS cells can be differentiated to a functional vascular cells and that human eTEBVs can be used to model diseases in vitro. This approach has been applied to other disease models.